Inflammation May Prevent Fat Burning
04 Jan 2017 --- Recent animal studies have shown that overweight mice can shed excess weight by converting unwanted white fat cells into energy-consuming brown slimming cells. However, new research now suggests that inflammatory responses that often occur in overweight people may be blocking this kind of fat cell conversion.
However, the researchers say they may have also found a starting point to bypass this inhibition, and are now looking into how this approach could be used to combat obesity in humans.
Published in the scientific journal “Cell Reports”, the study suggests that if body fat can simply be melted away with new active ingredients, then this could also prevent the widespread consequences of obesity – such as joint problems, diabetes and cardiovascular diseases.
The team around Alexander Pfeifer from the Institute of Pharmacology and Toxicology at the University of Bonn has been researching how this could be possible for years.
“In studies in mice, we have found various starting points to convert troublesome white fat cells into desirable brown fat cells,” reports Prof. Pfeifer.
The brown cells possess an extremely high number of mitochondria. These cell power stations “burn” white fat by converting it into thermal energy, which results in the number of brown cells increasing, and the mice losing significant amounts of weight.
The signal path of the messenger cyclic guanosine monophosphate (cGMP) plays an important role in this fat conversion.
“The desirable brown fat cells rely on cGMP,” notes Prof. Pfeifer. He explains that in various previous mice studies, that the widespread active ingredient sildenafil or a medication against pulmonary hypertension can be used to reduce the number of white fat cells to the benefit of the brown fat cells - thus accelerating fat burning like a turbocharger.
The researchers are looking into the possibility that this could effectively treat the significantly increasing obesity levels around the world, thus preventing serious complications.
They gave mice a high-calorie diet and examined the changes in the animals’ fat tissue. While hardly any inflammation occurred in the subcutaneous fat of obese mice, and cGMP signaling was largely intact, things were very different for the deeper-lying abdominal fat. Through the significant weight increase, inflammation had spread and the fat-burning turbocharger cGMP largely came to a standstill.
This uncovered a dual problem: abdominal fat is considered much more dangerous than subcutaneous fat because it triggers inflammation and can promote chronic conditions such as cardiovascular diseases.
According to the latest results from researchers at the University of Bonn, this is also where cGMP, which is important for fat-burning, was largely blocked. This lead the researchers to discover if it was possible to remove this block.
Lead author Abhishek Sanyal from Prof. Pfeifer’s team investigated in what way inflammation inhibits the cGMP signal path: “Tumor necrosis factor alpha (TNFalpha) plays an important role here,” reports Sanyal.
“The inflammation factor TNFalpha suppresses the cGMP signal path and thus prevents white fat cells from being turned into brown fat cells.”
Using human subcutaneous and abdominal fat samples, the scientists, in cooperation with the University Hospital Leipzig and the Karolinska Institutet Stockholm (Sweden), found similar changes not only to rodents but also to the human organism.
Although applications for obesity treatments in humans are still a long way off, the results indicate a direction for further research.
“Obviously, one possible starting point in combatting obesity could be to inhibit the inflammatory response in abdominal fat while administering cGMP-stimulating active ingredients,” summarizes Prof. Pfeifer.
